MYOCARDIAL-INFARCTION

Ischemia
Is any reduction in blood flow.
3 Features:
1. ↓ O2 supply
2. ↓ other nutrients
3. Impaired excretion of metabolic waste
*Imbalance between O2 supply and O2 demand

Arteriosclerosis
Walls of the arteries hardens –Loose elasticity

Risk factors:
Aging
Unhealthy diet
Obesity
HPN
Smoking
Arteriosclerosis
Monckeberg medial calcific sclerosis Atherosclerosis Arteriolosclerosis
↑ 50 y/o male Formation fibro-fatty plaque
Involves tunica media Involves tunica intima Occurs in smaller arteries
Medium sized arteries Medium-large size arteries Drug induced: Topical Calcineurin
Inhibitors (TCI’s)
Angina Pectoris
♥ muscles does not get as much as O2 rich blood as it needs.

Ischemia to the ♥ muscles
* It is not a dse But rather it is a sx of a ♥ dse.
Causes:
CAD
Coronary microvascular dse
Spasm of coronary arteries/arterioles
- constricted arteries, atherosclerosis, ↑LDL, smoking, cocaine
Types of Angina Pectoris
Stable Angina
Most common
70% blocked by plaque
Hypertrophic cardiomyopathy
↑ demand of O2
Stable Angina
Sub-endocardium Ischemia
Substernal chest pain/discomfort lasting 15-30 mins.
Squeezing/tightness/pressure like in the chest.
Radiating to neck, jaw, down the arms, back, belly.
Provoke by exertion, exercise, or emotional stress.
Relieved by rest or NTG
SOB
diaphoresis
Stable Angina
ECG/EKG:
ST segment depression
V4,V5,V6
Inverted T waves
Unstable Angina
Worsening, new onset of previous Angina

Cause: Rupturing of dynamic plaque
♥ tissue is ischemic
Unstable Angina
Retrosternal chest pain lasts for 30 mins

*Chest pain that doesn’t go away
Burning sensation/ pressure
Dyspnea at rest, or with exertion
MYOCARDIAL
INFARCTION
Definition
▪ refers to the process

by which areas of
myocardial cells in the
heart are permanently
destroyed.
▪ Heart attack
MI
Causes:
CAD
Damage to coronary artery
*Localized areas of necrotic tissue in the ♥

MI
TIME IS A TISSUE !!!
♥ Tissue begins to infarct approximately 20 mins after arterial blockage.
♥ tissue can be saved if blood flow can be restored within 4 hrs. of arterial blockage
Coronary artery spasm due
Atherosclerosis to cocaine or hypertension
Blockage in coronary
artery
Reduced blood flow in the heart

(ISCHEMIA)
Reduced oxygen in the heart
Necrosis of heart muscles

Signs and symptoms
▪ Pain
▪ Client may experience crushing substernal pain.
▪ Pain may radiate to the jaw, back, and left arm.
▪ Pain may occur without cause, primarily early in the morning.
▪ Pain is unrelieved by rest or nitroglycerin and is relieved only by opioids. e.
Pain lasts 30 minutes or longer
▪ Nausea and vomiting
▪ Diaphoresis
▪ Dyspnea
▪ Dysrhythmias
▪ Feelings of fear and anxiety
▪ Pallor, cyanosis, coolness of extremities
Naming MI by location
L circumflex occlusion
Lateral/posterior MI
L anterior descending occlusion

Most common
“Widow-maker”
Anterior wall damage
Depolarization
Starts at the SA node.
Changing the electrical charge of
the myocytes from (-) to (+)
♥ to contract
Repolarization
♥ relaxation phase
The myocytes goes back to its (-)
charged state
P wave
Represents atrial depolarization.
When the valves between the atria
and ventricles open, 70% of the
blood in the atria falls through with
the aid of gravity
QRS complex
It corresponds to the depolarization
of the right and left ventricles of the
heart
ST segment
Represents the interval between
ventricular depolarization and
repolarization.
T wave
Causes ventricular repolarization of
the heart in anticipation of the next
contraction.
Classification of MI
NSTEMI
Shows ST segment depression in ECG

Can be caused by reversible myocardial
ischemia
Classification of MI
STEMI
Shows ST segment elevation in ECG

♥ experiences more damage
Worse prognosis
Cardiac Enzymes(Cardiac markers)
▪ ECHOCARDIOGRAM
▪ Creatine Kinase and Its Isoenzymes (CK-MB)
▪ Peak elevation occurs 18 hours after the onset of chest pain and
returns to normal 48 to 72 hours later.
▪ Non-specific
▪ Myoglobin
▪ Level rises within 2 hours after cell death, with a rapid decline in the
level after 7 hours.
▪ Early marker/ non-specific
▪ Troponin I
▪ Level rises within 3 hours and remains elevated for up to 7 to 10 days.
▪ Nursing Responsibility: Monitor & refer upward result.
Cardiac Diagnostics
Heart Catheter + Xray

▪ Dye will be injected into C. artery.
▪ Locates any blockages, damage ♥ muscle & if C. artey can be
opened.
Stress Test w/ Myocardial Perfusion Imaging
Assess ♥ response to exercise & evaluate blood flow to the
myocardium (Threadmill)
Fractional Flow Reserve (FFR)
Check the BP & blood flow in C. artery.
Compare the ↑est possible blood flow w/ & w/out a blockage.
Medical Management
▪ PHARMACOLOGIC THERAPY
▪ Thrombolytics is to dissolve and lyse the
thrombus in a coronary artery (thrombolysis),
allowing blood to ﬂow through the coronary
artery again (reperfusion), minimizing the size of
the infarction, and preserving ventricular
function.
▪ streptokinase (Kabikinase, Streptase), alteplase
(Activase), and reteplase (r-PA, TNKase). Anistreplase
(Eminase) is another thrombolytic agent that may be
used.
▪Analgesics.
▪analgesic of choice for acute MI is
morphine sulfate (Duramorph,
Astramorph)
▪Angiotensin-Converting Enzyme
Inhibitors (ACE-I). *pril
SURGICAL MANAGEMENT
▪Emergent
percutaneous
coronary
intervention
(PCI)
NURSING MANAGEMENT
▪ Obtain a description of the chest discomfort.

▪ Administer oxygen and institute pain relief measures (morphine, nitroglycerin as
prescribed).
▪ Assess vital signs and cardiovascular status and maintain cardiac monitoring.
▪ Assess respiratory rate and breath sounds for signs of heartfailure
▪ Ensure bed rest and place the client in a semi Fowler’s position
▪ Establish an IV access route.
▪ Obtain a 12-lead ECG.
▪ Assess distal peripheral pulses and skin temperature

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Ischemia

Is any reduction in blood flow.

*Imbalance between O2 supply and O2 demand

Walls of the arteries hardens –Loose elasticity

Monckeberg medial calcific sclerosis Atherosclerosis Arteriolosclerosis

↑ 50 y/o male Formation fibro-fatty plaque

Involves tunica media Involves tunica intima Occurs in smaller arteries

♥ muscles does not get as much as O2 rich blood as it needs.

Worsening, new onset of previous Angina

Retrosternal chest pain lasts for 30 mins

▪ refers to the process

*Localized areas of necrotic tissue in the ♥

TIME IS A TISSUE !!!

♥ Tissue begins to infarct approximately 20 mins after arterial blockage.

Reduced blood flow in the heart

Reduced oxygen in the heart

Necrosis of heart muscles

L anterior descending occlusion

Shows ST segment depression in ECG

Shows ST segment elevation in ECG

Heart Catheter + Xray

▪ Obtain a description of the chest discomfort.

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